ライフサイエンスコーパス: baroreflex

1 s and enhanced the gain of the fetal cardiac baroreflex.

2 Thus, its upregulation does not augment the baroreflex.

3 iating dorsal PAG modulation of the arterial baroreflex.

4 minate dorsal PAG attenuation of the cardiac baroreflex.

5 echanical and neural aspects of the arterial baroreflex.

6 ndent of central command and/or the arterial baroreflex.

7 apnea incidence, and desensitization of the baroreflex.

8 hanism may be sympathetic activation via the baroreflex.

9 Following baroreflex ablation with trimethaphan (3-7 mg min(1)), c

10 2) the systolic blood pressure threshold for baroreflex activation increases significantly (the baror

11 Carotid baroreflex activation lowers blood pressure and might ha

12 We sought to determine the effect of baroreflex activation therapy (BAT) on systolic blood pr

13 roaches, transcatheter renal denervation and baroreflex activation therapy, are used in clinical prac

14 hypothesized that selective manipulation of baroreflex activity through electrical carotid sinus sti

15 expression of nNOS in the NTS of rats whose baroreflex activity was then studied.

16 The arterial baroreflex acts to buffer acute changes in blood pressur

17 a novel regulatory function of FGF21 in the baroreflex afferent pathway (the nucleus tractus solitar

18 ontrol of blood pressure regulations through baroreflex afferent pathway in HFD rats.

19 the circulation, and a decreased gain of the baroreflex, all indicative of an impaired baroreceptor r

20 al chemoreflex, diving response and arterial baroreflex, allowing the discrimination of muscle vasoco

21 rophenylalanine (p-CPA) on the cardiac vagal baroreflex and cardiopulmonary reflex in awake and anest

22 served increase in the reflex sensitivity of baroreflex and chemoreflex in in situ preparation.

23 NOS, resulting in activation of the arterial baroreflex and subsequent inhibition of central sympathe

24 ho-inhibitory and bradycardiac components of baroreflex and the sympathetic and respiratory responses

25 , the first synaptic station of afferents of baroreflexes and chemoreflexes, were evaluated using bra

26 pect to RVR, neural occlusion occurs between baroreflexes and the muscle mechanoreflex.

27 solitarii (NTS) of rat, attenuates arterial baroreflexes, and leads to lability of arterial blood pr

28 ese data suggest that attenuated sympathetic baroreflexes are the result of altered central mechanism

29 involves attenuation of the parasympathetic baroreflex as it persists in the presence of atenolol.

30 t the rostral-ventrolateral medulla, altered baroreflex blood pressure regulation and death from stro

31 intravenous trimethaphan) and less effective baroreflex buffering (BRB) of BP (potentiation of the sy

32 capnia also causes resetting of the arterial baroreflex, but that this resetting would not occur with

33 minance, and (iii) resetting of the arterial baroreflex causes immediate exercise-onset reflexive inc

34 Carotid baroreflex (CBR) function was determined using 5 s pulse

35 During each condition, carotid baroreflex (CBR) function was determined using the rapid

36 ance of the cardiac component of the carotid baroreflex (CBR) in control of blood pressure during iso

37 s immunoreactivity (Fos-IR) in the hindbrain baroreflex circuit.

38 nerves identify the cardiac parasympathetic baroreflex component as being active over a higher range

39 , we hypothesized that mechanical and neural baroreflex components contribute equally to baroreflex h

40 ctivity, and (3) if mechanical and/or neural baroreflex components related to differences in integrat

41 n centres) and the tonically active arterial baroreflex contribute importantly to cardiovascular cont

42 hich was accompanied by improvements in both baroreflex control and spectral indicators of cardiac sy

43 ed in the NTS have the potential to modulate baroreflex control at this site in the central barorefle

44 e B (TrkB) receptor signalling in the NTS on baroreflex control both in healthy and CHF rats.

45 arterial pressure and MSNA, but sympathetic baroreflex control is reduced before presyncope; (2) wit

46 Thus, other factors rather than sympathetic baroreflex control mechanisms contribute to sex differen

47 mechanisms will improve the understanding of baroreflex control of arterial blood pressure under this

48 itarius (NTS) is essential for orchestrating baroreflex control of blood pressure.

49 ypothesis that heat stress enhances arterial baroreflex control of burst gating and area.

50 Administration of E2 increased baroreflex control of heart rate (derived from the modif

51 o 22.4+/-2.1% of maximum, P<0.05), increased baroreflex control of heart rate (gain(max), 1.6+/-0.3 t

52 essure (MAP) but did significantly attenuate baroreflex control of heart rate (HR) evoked by low freq

53 The baroreflex control of heart rate (HR) is reduced followi

54 Baroreflex control of heart rate (n = 16) and muscle sym

55 ptors with isocapnic hypoxia resets arterial baroreflex control of heart rate and sympathetic vasocon

56 -3 mm Hg) and HR (33+/-3 bpm) and attenuated baroreflex control of HR at both ADN stimulation frequen

57 he nucleus ambiguus (NA) plays a key role in baroreflex control of HR, we examined whether CIH remode

58 None of the treatments altered MAP, HR, or baroreflex control of HR.

59 al LSNA (to 228 +/- 28% control) and gain of baroreflex control of LSNA (from 3.8 +/- 1.1 to 7.4 +/-

60 i.c.v. insulin infusion increased basal and baroreflex control of LSNA and HR similarly in pro-oestr

61 eases lumbar (LSNA) and renal (RSNA) SNA and baroreflex control of LSNA and RSNA in alpha-chloralose

62 otherwise untreated rats increased basal and baroreflex control of LSNA, indicating that endogenous N

63 ies indicate that insulin increases arterial baroreflex control of lumbar sympathetic nerve activity;

64 t rest, whole-body heating enhanced arterial baroreflex control of MSNA through increased sensitivity

65 The sensitivity of baroreflex control of MSNA was unchanged during DEH comp

66 To assess whether CO is related to arterial baroreflex control of MSNA, we constructed a baroreflex

67 mine the gain (i.e. sensitivity) of arterial baroreflex control of MSNA.

68 plasma insulin enhance the gain of arterial baroreflex control of MSNA.

69 (modified Oxford test) were used to evaluate baroreflex control of MSNA.

70 been used to describe two sites for arterial baroreflex control of MSNA.

71 lex mechanism, we tested the hypothesis that baroreflex control of muscle sympathetic nerve activity

72 We tested the hypothesis that baroreflex control of muscle sympathetic nerve activity

73 Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean ar

74 annabinoids (endocannabinoids) in regulating baroreflex control of RSNA through actions in the NTS.

75 contrast, i.c.v. leptin increased basal and baroreflex control of splanchnic SNA (SSNA) and heart ra

76 relationship between cardiac output (CO) and baroreflex control of sympathetic activity by measuring

77 rat medial nTS (mnTS), a region critical for baroreflex control of sympathetic outflow, produced dose

78 Prior studies investigating carotid baroreflex control of the cutaneous vasculature have yie

79 Baroreflex control of the heart rate is significantly re

80 <0.05) and increased the maximal gain of the baroreflex curves for heart rate (2.2+/-0.2 to 4.6+/-0.7

81 logical control system, such as the arterial baroreflex, depends critically upon both the magnitude (

82 g the central alterations that contribute to baroreflex desensitization during CHF.

83 The baroreflex desensitization in CHF is at least partly the

84 that contributes to sympatho-excitation and baroreflex desensitization.

85 uring short bouts of HG is not influenced by baroreflex disengagement.

86 ole in arterial pressure maintenance via the baroreflex during acute orthostasis in humans.

87 greater neural component of the sympathetic baroreflex during both pressure falls and pressure rises

88 bles were related to the presence/absence of baroreflex dysfunction (defined by spontaneous barorefle

89 were more frequent in surgical patients with baroreflex dysfunction (relative risk, 1.66 [95% CI, 1.1

90 acic echocardiography following experimental baroreflex dysfunction (sino-aortic denervation) in rats

91 We hypothesized that baroreflex dysfunction alone is sufficient to cause card

92 eceptor kinase 2 expression in conditions of baroreflex dysfunction and preserved cardiac function.

93 Baroreflex dysfunction in patients was also associated w

94 Experimental baroreflex dysfunction in rats and mice resulted in impa

95 Baroreflex dysfunction was present in 81 of 249 patients

96 The associations of baroreflex dysfunction with intraoperative cardiac funct

97 Because of baroreflex engagement, the magnitude of the response is

98 he horse fetus, with particular relevance to baroreflex function and hind limb vascular arterial reac

99 re evaluated for heritable autonomic traits: baroreflex function and pressor response to environmenta

100 gnalling in the dmNTS is integral for normal baroreflex function as indicated by the blunting of baro

101 smitters and neuromodulators in the dmNTS on baroreflex function both in normal and CHF states is not

102 were differences in sympathetic activity and baroreflex function by age, sex, or physical activity st

103 ermine if resetting of the carotid-vasomotor baroreflex function curve during exercise is modulated b

104 comparison to control, the carotid-vasomotor baroreflex function curve was relocated downward and lef

105 gal control of the heart rate and attenuated baroreflex function during aging.

106 lved in descending modulation of the cardiac baroreflex function during defensive behavior.

107 entional wisdom, hysteresis in cardiac vagal baroreflex function exhibits a specific pattern: pressur

108 stem, without changing intrinsic sympathetic baroreflex function in elderly hypertensive patients.

109 of arterial pressure and impairment of vagal baroreflex function in space.

110 Impairment of baroreflex function is associated with the progression o

111 Baroreflex function is impaired in patients with obstruc

112 of vasomotor responsiveness and sympathetic baroreflex function is not the cause of neurally mediate

113 oth peripheral and central chemoreceptors on baroreflex function may contribute to promoting hyperten

114 ysical activity status, (2) if any aspect of baroreflex function related to differences in resting sy

115 flex activation increases significantly (the baroreflex function shifts to the right; 120 +/- 14 vs.

116 Cardiac vagal baroreflex function was assessed using the modified Oxfo

117 Baroreflex function was determined using the modified Ox

118 Baroreflex function was further assessed during a Valsal

119 Blood pressure and baroreflex function was reduced in double knockout mice,

120 Baroreflex function was similar between groups.

121 to measure sympathetic, parasympathetic, and baroreflex function.

122 oreceptors does not appear to alter arterial baroreflex function.

123 PAG-evoked increases in MAP, HR and cardiac baroreflex function.

124 crease in sympathetic drive and resetting of baroreflex function.

125 noeas (RHA) produces prolonged impairment in baroreflex function.

126 hypertension and restored ACE2 activity and baroreflex function.

127 vasopressor response to Ang II and impaired baroreflex function.

128 his difference in the operating range of the baroreflex-function curves is exaggerated in the spontan

129 /- 19, 6 nU; and 205 +/- 28, 60 nU) and LSNA baroreflex gain (in % control mmHg-1 from 4.3 +/- 1.2 to

130 explore the explanatory power of integrated baroreflex gain and its mechanical and neural components

131 Baroreflex gain and its mechanical and neural components

132 the antagonization of TrkB, which inhibited baroreflex gain and range.

133 etrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations (r

134 etrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations ro

135 e the sympathetic nervous system and enhance baroreflex gain are well known, the specific brain site(

136 rvals declined by 14% (P = 0.003), and vagal baroreflex gain by 9% (P = 0.009).

137 resting sympathetic outflow nor sympathetic baroreflex gain components.

138 ; altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve bu

139 Sympathetic baroreflex gain may be reduced, and muscle sympathetic f

140 ivity (LSNA) were recorded continuously, and baroreflex gain of HR and LSNA were measured before and

141 Baroreflex gain was not altered by hyperpnoea or hyperca

142 This attenuation of the baroreflex gain was unaffected by subsequent anesthesia.

143 es ( approximately 0.25 Hz) lowered arterial baroreflex gain, and provoked smaller arterial pressure

144 the sympathetic nervous system and increase baroreflex gain, via a neural pathway that includes the

145 The baroreflex gain, whether calculated from the rise in pre

146 hown to either increase, or not change vagal baroreflex gain.

147 ponents related to differences in integrated baroreflex gain.

148 t in conjunction to determine differences in baroreflex gain.

149 ure, sympathetic vasoconstrictor outflow, or baroreflex gain.

150 flow to higher pressures, without changes in baroreflex gain.

151 ) inhibited both the cardiac and sympathetic baroreflex gains (16 +/- 5% and 59 +/- 11% of control, r

152 e) and non-cardiac sympathetic (T8-10 chain) baroreflex gains were obtained.

153 Baroreflex heart rate responses to phenylephrine-induced

154 ull expression of PEH requires a functioning baroreflex, hypertension, and activation of muscle affer

155 ls, and therefore it has been suggested that baroreflex hysteresis derives solely from vascular behav

156 baroreflex components contribute equally to baroreflex hysteresis.

157 responses to phenylephrine were enhanced and baroreflexes impaired in these animals.

158 red neurons and Ang II-induced inhibition of baroreflex in spontaneously hypertensive rats (SHR) vers

159 tudy examined whether attenuated sympathetic baroreflexes in OZRs may be due to altered sensory or ce

160 this confounding inhibitory influence of the baroreflex, in the current study we directly measured sk

161 n curves for the cardiac versus the vascular baroreflex indicates that there is a hierarchical recrui

162 ncrease in blood pressure (BP) and prolonged baroreflex inhibition of renal sympathetic nerve activit

163 the NTS were found to significantly prolong baroreflex inhibition of RSNA compared to control, simil

164 We found that the non-cardiac SNA baroreflex is active over a lower range of pressures tha

165 ence between the cardiac and non-cardiac SNA baroreflex is also seen in end-organ sympathetic outflow

166 n manifest as a complete dissociation of the baroreflex limbs at low pressures.

167 Arterial baroreflexes may regulate resistance vessels supplying g

168 blood pressure (BP) is regulated through the baroreflex mechanism, we tested the hypothesis that baro

169 Others have asked, If baroreflex mechanisms are functioning normally, how can

170 ear signals, potentially implicating central baroreflex mechanisms for anxiolytic treatment targets.

171 hesis that spaceflight does not impair human baroreflex mechanisms.

172 ual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea.

173 ctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, an

174 However, cardiovagal baroreflex-mediated bradycardia during a hypertensive st

175 l influences with atropine similarly reduced baroreflex-mediated bradycardic responses to increases i

176 ques may limit the ability to detect carotid baroreflex-mediated changes in cutaneous vascular conduc

177 Baroreflex-mediated changes in sympathetic vasomotor ton

178 Furthermore, E2 administration increases baroreflex-mediated heart rate responses to orthostasis

179 ower body negative pressure (LBNP; activates baroreflex-mediated sympathetic system) and the cold pre

180 Similarly, after meal intake, arterial baroreflex-MSNA gain for burst incidence and total MSNA

181 fasting insulin concentrations, the arterial baroreflex-MSNA gain remained unchanged.

182 le glucose was maintained constant, arterial baroreflex-MSNA gain was similarly enhanced (e.g. burst

183 lar resistance (SVR), possibly confounded by baroreflexes or interactions between single nucleotide p

184 insic inhibitory input to the neurons in the baroreflex pathway.

185 roreflex control at this site in the central baroreflex pathway.

186 hesis that nNOS is involved in excitation of baroreflex pathways in NTS while excluding pharmacologic

187 nNOS in the NTS is integral to excitation of baroreflex pathways involved in reflex tachycardia, a la

188 e too short and variable to be attributed to baroreflex physiology.

189 attenuated in habitual smokers; that is, the baroreflex plays a permissive role, allowing sympathoexc

190 We have examined the baroreflex pressure-function curves for changes in heart

191 to elicit sigmoid, vagally mediated carotid baroreflex R-R interval responses.

192 creasing CBV and loading the cardiopulmonary baroreflex reduces the magnitude of exercise-induced inc

193 ndently suppressed lumbar SNA (LSNA) and its baroreflex regulation, and these effects were blocked by

194 ulmonary baroreceptor load influence carotid baroreflex resetting during dynamic exercise.

195 effects were assessed by measuring the RSNA baroreflex response to increased pressure after bilatera

196 d chronotropic responses manifested the same baroreflex responses as animals that had been treated wi

197 In order to test this hypothesis, baroreflex responses were studied in adult, urethane-ane

198 hibitory effects resulting in attenuation of baroreflex responses, on the other, are discussed.

199 Neither AAV2 eGFP nor AAV2nNOScDNA affected baroreflex responses.

200 e influence of ageing on the latency of peak baroreflex responses.

201 -2 (0.4 mmol/l) into the mNTS attenuated the baroreflex responses.

202 st) into the mNTS (0.5 mmol/l) did not alter baroreflex responses.

203 rons by E-2 may result in an exaggeration of baroreflex responses.

204 f mu-opioid receptors in the mNTS attenuates baroreflex responses.

205 ticularly important and occurs via augmented baroreflex responsiveness and increased cardiomyocyte se

206 ents (muscle metaboreflex) decreases cardiac baroreflex responsiveness during leg cycling exercise in

207 an cortisol better determined heart rate and baroreflex responsiveness in the equine fetus.

208 m, mean and maximum (+/-s.d.) supine control baroreflex sensitivities averaged 5 +/- 3, 18 +/- 6, and

209 fferences in the cardiovagal and sympathetic baroreflex sensitivities between phases under any condit

210 antecedent hypoglycemia leads to 1) reduced baroreflex sensitivity (16.7 +/- 1.8 vs. 13.8 +/- 1.4 ms

211 Baroreflex sensitivity (adjusted odds ratio, 0.9; p = 0.

212 systolic blood pressure, cardiac parameters, baroreflex sensitivity (BRS) and hyperinsulinemia in the

213 This study sought to evaluate cardiac baroreflex sensitivity (BRS) as a predictor of response

214 lex function as indicated by the blunting of baroreflex sensitivity (BRS) following the antagonizatio

215 Sympathetic baroreflex sensitivity (BRS) is greater during decreasin

216 Sympathetic baroreflex sensitivity (BRS) was assessed.

217 Baroreflex sensitivity (BRS) was quantified from the R-R

218 ventilatory recruitment threshold (VRT-CO2), baroreflex sensitivity (BRS), blood pressure, and blood

219 ailure (CHF) results in blunting of arterial baroreflex sensitivity (BRS), which arises from alterati

220 es in sympathetic activity and reductions in baroreflex sensitivity (BRS).

221 mental stress, as well as impaired arterial baroreflex sensitivity (BRS).

222 nism for the decrease in spontaneous cardiac baroreflex sensitivity (cBRS) during exercise in humans.

223 thetic nerve activity (MSNA) and sympathetic baroreflex sensitivity (MSNA-diastolic pressure relation

224 emetry), autonomic function, and spontaneous baroreflex sensitivity (SBRS) were not significantly dif

225 Fortunately, emerging data suggest that baroreflex sensitivity and autonomic function may be res

226 Baroreflex sensitivity and the sympathetic response to h

227 Cardiovagal baroreflex sensitivity assessed during decreasing BP (i.

228 The spontaneous baroreflex sensitivity at baseline was significantly low

229 Similar sympathetic baroreflex sensitivity between sexes and phases was also

230 at 0.6 of gestation; however, fetal cardiac baroreflex sensitivity decreased with advancing gestatio

231 ared with baseline euglycemic conditions, 1) baroreflex sensitivity decreases significantly (19.2 +/-

232 Sympathetic baroreflex sensitivity did not differ between sexes (P =

233 MSNA, haemodynamic responses and baroreflex sensitivity during early tilting were not dif

234 athetic neural responses but not sympathetic baroreflex sensitivity during orthostasis, though uprigh

235 t during brief periods of observation, human baroreflex sensitivity fluctuates widely and rhythmicall

236 Fast Fourier transforms indicated that baroreflex sensitivity fluctuations (expressed as percen

237 The periodicity of very low frequency baroreflex sensitivity fluctuations was not influenced s

238 rterial pressure, sympathovagal balance, and baroreflex sensitivity for control of heart rate.

239 mpathetic nerve activity and reduced cardiac baroreflex sensitivity heighten cardiovascular risk, alt

240 nin activity, aldosterone, urine sodium, and baroreflex sensitivity in both groups.

241 hough studies have examined resting arterial baroreflex sensitivity in older subjects, little attenti

242 mpathetic nerve activity and reduced cardiac baroreflex sensitivity in patients with RA compared to m

243 of ANA-12 into the dmNTS greatly diminished baroreflex sensitivity in sham rats, whereas it had less

244 s measurements of heart rate variability and baroreflex sensitivity in the neuromonitoring setting of

245 Sympathetic baroreflex sensitivity increased from supine to upright

246 Reduced baroreflex sensitivity is associated with nicotinamide a

247 Not only sympathetic but also cardiovagal baroreflex sensitivity is similar between sexes and mens

248 roreflex dysfunction (defined by spontaneous baroreflex sensitivity of <6 ms mm Hg).

249 Hypoxia had no significant effect on baroreflex sensitivity or 'set point' for the control of

250 Baroreflex sensitivity showed no correlation with intrac

251 Baroreflex sensitivity was assessed every 10 seconds usi

252 Baroreflex sensitivity was assessed in the time domain w

253 Sympathetic baroreflex sensitivity was quantified using the slope of

254 Sympathetic baroreflex sensitivity was quantified using the slope of

255 s measurements of heart rate variability and baroreflex sensitivity we aimed to test whether autonomi

256 s of RR interval variability and spontaneous baroreflex sensitivity were also computed.

257 t subjects, moderate ongoing fluctuations of baroreflex sensitivity were punctuated by brief major pe

258 Sympathovagal balance and spontaneous baroreflex sensitivity were restored during vitamin C in

259 Similar changes in baroreflex sensitivity were seen.

260 We estimated vagal baroreflex sensitivity with systolic pressure and R-R in

261 art rate variability, heart rate turbulence, baroreflex sensitivity) were significant predictors of a

262 We have previously shown that depressed baroreflex sensitivity, an established marker of reduced

263 ngiotensin II levels, inflammation, impaired baroreflex sensitivity, and autonomic dysfunction, as we

264 stress, impaired sympathetic and cardiovagal baroreflex sensitivity, and increased inflammation.

265 ormalized indexes of sympathetic outflow and baroreflex sensitivity, and reduced the incidence of apn

266 ween arrhythmic events and predictive tests (baroreflex sensitivity, heart rate turbulence, heart rat

267 Mean values of baroreflex sensitivity, heart rate variability, intracra

268 upled with impairments in renal function and baroreflex sensitivity, increased neuroinflammatory mark

269 eart rate variability, endothelial function, baroreflex sensitivity, inflammation, and platelet funct

270 t, as measured by heart rate variability and baroreflex sensitivity, is significantly associated with

271 function, including decreased cardiac vagal baroreflex sensitivity, may contribute directly to morta

272 stiffness; (2) it is associated with reduced baroreflex sensitivity, which increases blood pressure v

273 trual cycle had no influences on cardiovagal baroreflex sensitivity.

274 ssed according to heart rate variability and baroreflex sensitivity.

275 ivity and negatively correlated with cardiac baroreflex sensitivity.

276 renal sympathetic nerve activity and to test baroreflex sensitivity.

277 ors with a possible reduction in sympathetic baroreflex sensitivity.

278 heart, leading to hypertension and depressed baroreflex sensitivity.

279 an increase in parasympathetic activity and baroreflex sensitivity.

280 vs. sham-operated SHR) and an improvement in baroreflex sensitivity.

281 tatory or inhibitory role in transmission of baroreflex signals in the nucleus tractus solitarii (NTS

282 Fetal cardiac baroreflex slopes were obtained using the peak pressor a

283 w and previously published studies involving baroreflex stimulation and pharmacological blockade of t

284 nervation, cervical vagal nerve stimulation, baroreflex stimulation, cutaneous stimulation, novel dru

285 esia, low-level vagal nerve stimulation, and baroreflex stimulation.

286 t-term exposure to RHA shifts ('resets') the baroreflex stimulus-response curve to higher levels of B

287 Furthermore, we propose that baroreflex suppression of sympathetic activation is atte

288 ears, and a final follow-up: pharmacological baroreflex testing (baroreceptor reflex sensitivity), sh

289 terminant of MSNA in humans via the arterial baroreflex, the lack of correlation among individuals su

290 baroreflex control of MSNA, we constructed a baroreflex threshold diagram for each individual by plot

291 y and BRS was measured using the spontaneous baroreflex threshold technique.

292 a lower range of pressures than the cardiac baroreflex (threshold 66 +/- 1 mmHg versus 82 +/- 5 mmHg

293 othesis that endogenous AEA can modulate the baroreflex through cannabinoid CB(1) receptor activation

294 Baroreflex trials were separated by 30 min of rest.

295 the working heart-brainstem preparation, the baroreflex was activated using brief pressor stimuli and

296 t from both central command and the arterial baroreflex were eliminated.

297 In contrast, the operating points of the baroreflexes were shifted rightward (to higher levels of

298 hical recruitment of the output limbs of the baroreflex with a sympathetic predominance at lower arte

299 Both handgrip (HG) and disengagement of baroreflexes with lower body negative pressure (LBNP) ca

300 increase the gain of the cardiac limb of the baroreflex without changing the sympathoinhibitory compo